id:"swepub:oai:DiVA.org:umu-1680"
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- Janson, Veronica,1974-Umeå universitet,Institutionen för medicinsk biovetenskap (författare)
Cisplatin-resistance and cell death in malignant pleural mesothelioma cells
- BokEngelska2008
Förlag, utgivningsår, omfång ...
- Umeå :Medicinsk biovetenskap,2008
- 104 s.
- electronicrdacarrier
Nummerbeteckningar
- LIBRIS-ID:oai:DiVA.org:umu-1680
- ISBN:9789172645608
- https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1680URI
Kompletterande språkuppgifter
- Språk:engelska
- Sammanfattning på:engelska
Ingår i deldatabas
- SwePubSwePub
Klassifikation
Serie
- Umeå University medical dissertations,0346-6612 ;1192
Anmärkningar
- Malignant pleural mesothelioma (MPM) is an aggressive, treatment-resistant tumour. Cisplatin (cis-diamminedichloroplatinum (II)) is the best single-agent chemotherapy for MPM, but platinum-based combination therapies give the best overall response rates. However, cisplatin use is limited by resistance and severe side effects. This thesis has increased the knowledge concerning cisplatin-induced cell death in MPM by describing a novel potential therapeutic target, and three novel phenotypes of cisplatin-resistance in a human MPM cell line (P31) and its cisplatin-resistant sub-line (P31res1.2). The novel potential therapeutic target, and one of the novel phenotypes, was cisplatin-resistant pro-apoptotic BH3-only proteins. In the P31 cells, cisplatin transiently increased pro-apoptotic BH3-only proteins during 6 h of exposure. This response was almost completely abrogated in the P31res1.2 cells. De-regulated caspase activity and activation was the second novel phenotype identified. The P31res1.2 cells had earlier, possibly mitochondria-independent, caspase-3 activation, increased basal caspase-3 activity and increased basal cleavage of caspase-8 and -9. Despite these differences, 6-h equitoxic cisplatin exposures rendered 50-60% of the cells apoptotic in both cell lines. The third novel phenotype was abrogated Na+K+2Cl--cotransporter (NKCC1) activity. Although NKCC1 activity was dispensable for cisplatin-induced apoptosis, balanced potassium transport activity was essential for P31 cell survival. Finally, the survival signalling protein Protein Kinase B (PKB or Akt) isoforms α and γ were constitutively activated in a PI3K-independent manner in P31 cells. In the P31res1.2 cells, PKBα and γ activities were increased, and there was PI3K-dependent activation of PKBβ. However, this increase in PKB isoform activity was not strongly associated to the cisplatin-resistance of the P31res1.2 cells.
Ämnesord och genrebeteckningar
- MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Annan klinisk medicin hsv//swe
- MEDICAL AND HEALTH SCIENCES Clinical Medicine Other Clinical Medicine hsv//eng
- apoptosis
- BH3-only proteins
- caspase
- cell morphology
- potassium transport
- protein kinase B (PKB/Akt)
- signalling pathways
- time
- Clinical chemistry
- Klinisk kemi
Biuppslag (personer, institutioner, konferenser, titlar ...)
- Grankvist, Kjell,ProfessorUmeå universitet,Institutionen för medicinsk biovetenskap (preses)
- Henriksson, Roger,ProfessorUmeå universitet,Institutionen för strålningsvetenskaper (preses)
- Behnam-Motlagh, Parviz,PhDUmeå universitet,Institutionen för medicinsk biovetenskap (preses)
- Johansson, Anders,ODUmeå universitet,Institutionen för odontologi (preses)
- Zhivotovsky, Boris,ProfessorInstitutet för Miljömedicin, Toxikologi, Karolinska Institutet, Stockholm (opponent)
- Umeå universitetInstitutionen för medicinsk biovetenskap (creator_code:org_t)
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